-
- Kwun Wah Wen
- Department of Pathology and Helen Diller Family Comprehensive Cancer Center University of California San Francisco CA USA
-
- Linlin Wang
- Department of Laboratory Medicine University of California San Francisco CA USA
-
- Joshua R. Menke
- Department of Pathology Stanford University Palo Alto CA USA
-
- Blossom Damania
- Department of Microbiology & Immunology & Lineberger Comprehensive Cancer Center University of North Carolina Chapel Hill NC USA
抄録
<jats:p>Epstein–Barr virus (EBV; human herpesvirus 4; HHV‐4) and Kaposi sarcoma‐associated herpesvirus (KSHV; human herpesvirus 8; HHV‐8) are human gammaherpesviruses that have oncogenic properties. EBV is a lymphocryptovirus, whereas HHV‐8/KSHV is a rhadinovirus. As lymphotropic viruses, EBV and KSHV are associated with several lymphoproliferative diseases or plasmacytic/plasmablastic neoplasms. Interestingly, these viruses can also infect epithelial cells causing carcinomas and, in the case of KSHV, endothelial cells, causing sarcoma. EBV is associated with Burkitt lymphoma, classic Hodgkin lymphoma, nasopharyngeal carcinoma, plasmablastic lymphoma, lymphomatoid granulomatosis, leiomyosarcoma, and subsets of diffuse large B‐cell lymphoma, post‐transplant lymphoproliferative disorder, and gastric carcinoma. KSHV is implicated in Kaposi sarcoma, primary effusion lymphoma, multicentric Castleman disease, and KSHV‐positive diffuse large B‐cell lymphoma. Pathogenesis by these two herpesviruses is intrinsically linked to viral proteins expressed during the lytic and latent lifecycles. This comprehensive review intends to provide an overview of the EBV and KSHV viral cycles, viral proteins that contribute to oncogenesis, and the current understanding of the pathogenesis and clinicopathology of their related neoplastic entities.</jats:p>
収録刊行物
-
- The FEBS Journal
-
The FEBS Journal 289 (24), 7631-7669, 2021-10-02
Wiley